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Updated: Oct 16, 2025

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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
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IL-23 orchestrating immune cell activation in arthritis
Aurélie Najm1, Iain B McInnes1
1Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
Rheumatology (Oxford, England)
|October 20, 2021
Summary
Interleukin-23 (IL-23) drives Th17 cell differentiation, crucial for inflammatory arthritis pathogenesis. Targeting IL-23 shows promise for psoriatic arthritis (PsA) but needs further investigation for rheumatoid arthritis (RA).
Area of Science:
- Immunology
- Cytokine Biology
- Rheumatology
Background:
- Interleukin-23 (IL-23) is a pro-inflammatory cytokine central to innate and adaptive immunity.
- It promotes T helper 17 (Th17) cell differentiation, a key factor in rheumatic disease pathogenesis.
- Pre-clinical models highlight IL-23's critical role in arthritis development.
Discussion:
- IL-23-induced Th17 cells secrete IL-17A and other cytokines, contributing to synovial and skin inflammation in psoriatic arthritis (PsA).
- The role of IL-23 in rheumatoid arthritis (RA) pathogenesis is also suggested.
- Therapeutic strategies targeting IL-23 have demonstrated efficacy in PsA treatment.
Key Insights:
- IL-23 is a critical cytokine in the development and maintenance of inflammatory arthritis.
- Th17 cells, regulated by IL-23, are key mediators of inflammation in conditions like PsA.
- Targeting IL-23 is an effective therapeutic strategy for PsA.
Outlook:
- Further research is needed to establish the efficacy of IL-23 inhibition in rheumatoid arthritis (RA).
- Investigating IL-23's precise role in RA pathogenesis may reveal new therapeutic avenues.
- Continued exploration of IL-23 targeted therapies holds potential for managing inflammatory arthritic conditions.
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